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Prof. Khalifa Sifaw Ghenghesh Dept. of Medical Microbiology, Faculty of Medicine, Tripoli University, Tripoli-Libya بسم الله الرحمن الرحيم BACTERIAL PATHOGENESIS.

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Presentation on theme: "Prof. Khalifa Sifaw Ghenghesh Dept. of Medical Microbiology, Faculty of Medicine, Tripoli University, Tripoli-Libya بسم الله الرحمن الرحيم BACTERIAL PATHOGENESIS."— Presentation transcript:

1 Prof. Khalifa Sifaw Ghenghesh Dept. of Medical Microbiology, Faculty of Medicine, Tripoli University, Tripoli-Libya بسم الله الرحمن الرحيم BACTERIAL PATHOGENESIS

2 The Pathogen: A Disease Producing Microorganism. Pathogenicity: Capacity to Initiate Disease. Virulence: Capacity to Harm the Host. Refer to Degree of Pathogenicity. Opportunistic Pathogens: Common or Non Pathogenic Microbes. e.g. Normal Flora of the Body.

3 Infection: The Lodgement and Multiplication of a Parasite in or on the Tissues of a Host. Disease: A Rare Consequence of Infection. Measurement of Virulence: The Median Lethal Dose (LD50) is Used. Number of Microorganisms or Micrograms of Toxin Required to Kill 50% of Infected Animals.

4 Koch's Postulates Isolated diseased not healthy people Growth pure culture Induce disease susceptible animals Re-isolated susceptible animals

5 Virulence factors (Determinants of pathogenicity) Number of initial organisms Immune status PATHOGENICITY

6 VIRULENCE FACTORS

7 Virulence factors help bacteria to: Invade the host, Cause disease, and Evade host defenses.

8 1. Toxigenicity Tissue injury: Exotoxins: Include several types of protein toxins and enzymes produced and/or secreted from pathogenic bacteria. Include cytotoxins, neurotoxins, and enterotoxins.

9 Endotoxins: Lipopolysaccharide Gram-negative bacteria Endotoxic (Septic) Shock: Hypotension (tissue pooling of fluids) Disseminated intravascular coagulation Fever Lack of effective oxygenation Overall system failure

10 Differentiation of Exotoxins and Endotoxins. Exotoxins Endotoxins --------------------------------------------------------------------------------------- -Excreted by living cells.-Released after death of bacteria. -Relatively unstable.-Relatively stable. -Highly antigenic; -Do not stimulate formation stimulate the formation of antitoxin. of high-titer antitoxin. -Converted into antigenic, -Not converted into toxoids. nontoxic toxoids. -Highly toxic.-Weakly toxic. -Do not produce -Often produce fever fever in host. in host.

11 2. Invasiveness Capacity of a pathogen to spread in the host tissues after establishing infection. Surface components that allow the bacterium to invade host cells can be encoded on plasmids, but more often are on the chromosome.

12 Penetration and spread Vibrio cholerae Salmonella enteritidis Salmonella typhi Epithelium

13 3. Capsules Antiphagocytic structures Polysacchride

14 The Relatively Stable, Irreversible Attachment of Bacteria to a Surface. Fimbrial Adhesins Nonfimbrial Proteinaceous Adhesins. 4. Adhesion

15 adhesin EPITHELIUM receptor BACTERIUM

16 E. coli with fimbriae (Pili)

17 5. Siderophores Iron-binding factors that allow some bacteria to compete with the host for iron, which is bound to hemoglobin, transferrin, and lactoferrin.

18 6. Other Aggressions Mainly Enzymes: Hyaluronidase >> Spreading Factor. Coagualse >> Thrombin - Like Enzyme. Fibrinolysin >> Streptokinase. Proteases >> Hydrolyse Immunoglobulins. Others


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